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Article

Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2).

The Journal of biological chemistry - 21 Jun 2013

Chiluiza David, Krishna Sneha, Schumacher Valérie A, Schlöndorff Johannes

Abstract excerpt

Gain-of-function mutations in the canonical transient receptor potential 6 (TRPC6) gene are a cause of autosomal dominant focal segmental glomerulosclerosis (FSGS). The mechanisms whereby abnormal TRPC6 activity results in proteinuria remain unknown. The ERK1/2 MAPKs are activated in glomeruli and podocytes in several proteinuric disease models. We therefore examined whether FSGS-associated mutations in TRPC6...

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Source

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Identifiers

PMID: 23645677
DOI: 10.1074/jbc.M113.463059
PMCID: PMC3689983

Genes

TRPC6
EGF

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2).PMID 23645677Read ↗

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